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Norepinephrine (NE) and intermittent hypoxia (IH) impact short term synaptic plasticity in the hippocampus
Author(s) -
Barnard Jasmine E,
Khuu Maggie A,
Garcia Alfredo J
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.841.5
Subject(s) - excitatory postsynaptic potential , hippocampal formation , population , hypoxia (environmental) , neuroplasticity , norepinephrine , hippocampus , neuroscience , medicine , endocrinology , anesthesia , chemistry , psychology , inhibitory postsynaptic potential , dopamine , environmental health , organic chemistry , oxygen
Conditions such as sleep apnea can produce states of increased noradrenergic tone that coincide with bouts of IH. A previous report indicates that the influence of IH on neurophysiology is changed by increased noradrenergic tone. The objective of this ongoing study is to determine how acute IH (AIH) and NE affect short‐term synaptic plasticity (i.e., paired pulse facilitation, PPF) in the CA1 neuronal population. We hypothesize that NE changes PPF following AIH. To test this hypothesis, extracellular recordings of electrically evoked field excitatory postsynaptic potentials were made from the CA1 neuronal population within mouse hippocampal brain slices. A paired pulse protocol using an interpulse interval (20ms to 500ms) was performed before and following AIH. AIH consisted of three intervals of hypoxia (95% N2, duration=180 sec) separated by recovery periods (95% O2, duration=180 sec). While 2 mircoM NE did not affect PPF (n=3), PPF was augmented following AIH (n=4). However, combined, NE/AIH suppressed PPF (n=3). Our findings, to date, suggest that NE alters how IH affects short term plasticity in the CA1 neuronal population.